Our results are consistent with the supposition that both Aβ and tau are necessary for memory decline in the preclinical stages of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Currently, over five million Americans suffer with Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[ 18 F]PI-2620 was selected for clinical validation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Parkinson's disease (PD) is the second most common degenerative disorder. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes, oligodendrocytes, and microglia are abundant cell types found in the central nervous system and have been shown to play crucial roles in regulating both normal and disease states. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current technological advancements in clinical and research settings have permitted a more intensive and comprehensive understanding of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
OCT measurements did show significant decrease in temporal, nasal, inferiorR (R means examination of retina in two sections as superior and inferior instead of four quadrants) RNFL thickness and foveal, parafoveal, macular thickness of AD group compared to control group. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
FTP and thickness were differentially related to cognitive performance in several domains. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Retention of 18F-Flortaucipir is reportedly increased in the semantic variant of primary progressive aphasia (svPPA), which is dominated by TDP-43 pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite the presence of abundant tau aggregates in multiple regions in all CTE brains, only faint or no [18F]-AV-1451 binding signal could be detected by autoradiography. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[18F]AV-1451 is one of the most widely used radiotracers for positron emission tomography (PET) imaging of tau protein aggregates in neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Regional standardized uptake value ratios (SUVRs) for tau positron emission tomography (PET) were compared among 19 cognitively normal human immunodeficiency virus (HIV)-negative control individuals, 20 HIV-negative patients with symptomatic Alzheimer disease, 15 cognitively normal HIV-positive individuals, and 17 cognitively impaired HIV-positive individuals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggested that occipitoparietal cortex, posterior cingulate cortex and precuneus, which were particularly affected by increased tau accumulation in VS-AD patients, may associate with visuospatial dysfunction of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Following the conversion of FBB or FMM SUVRs into CL units, a direct relationship was formed between the FBB or FMM SUVRs and the CL units using dcCL method (FBB dcCL = 151.42 × FBB dcSUVR - 142.24 and FMM dcCL = 148.52 × FMM dcSUVR - 137.09). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Studies generally indicate a progressive impairment in DMN connectivity during the course of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found that education level was positively associated with a wide range of complex cognitive domains including general mental status, episodic memory, language, attention, executive function and visuospatial processing, and it showed significantly negative correlations with FC of multiple areas in the Default Mode Network (DMN) and Left Frontal-parietal Network (LFP) which are related to complex cognition. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mild cognitive impairment is defined as greater cognitive decline than expected for a person at a particular age and is sometimes considered a stage between healthy aging and Alzheimer's disease or other dementia syndromes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulating evidence suggests that memory is impaired in posterior cortical atrophy (PCA), alongside the early and defining visual disorder. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Using AI for dementia diagnosis is still in research stage, however some of the work points to the development of new medical devices. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The default-mode network (DMN) and its principal core hubs in the posterior midline cortices (PMC), i.e., the precuneus and the posterior cingulate cortex, play a critical role in the human brain structural and functional architecture. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Many ocular diseases (such as glaucoma, diabetic retinopathy, age-related macular degeneration, and traumatic eye injuries) can result in the degeneration of retinal cells and the subsequent loss of vision. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In terms of the retinal neuronal structure, multiple retinal neuronal layers are significantly thinner in Alzheimer's disease dementia, such as the parapapillary retinal nerve fiber layer (RNFL) and macular ganglion cell-inner plexiform layer (GC-IPL). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Homocysteine (Hcy), a sulfur-containing nonproteinogenic amino acid, is generated as a metabolic intermediate. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
It could be shown that Alzheimer type dementia, Parkinson's disease, multiple sclerosis. cerebral infarction and CADASIL are neuronal diseases with rarification of retinal vessels and atrophy of the retinal layers in the ocular fundus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Complement pathway overactivation can lead to neuronal damage in various neurological diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
How the 0–100 score works — and why some entries are capped
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →